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      Abnormal splicing of the leptin receptor in diabetic mice.

      Nature

      Tissue Distribution, Alternative Splicing, Receptors, Leptin, Receptors, Cell Surface, Proteins, Polymerase Chain Reaction, Mutation, Molecular Sequence Data, Mice, Inbred C57BL, Mice, Leptin, genetics, Diabetes Mellitus, Experimental, DNA Primers, Chromosome Mapping, Carrier Proteins, Base Sequence, Animals, Amino Acid Sequence

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          Abstract

          Mutations in the mouse diabetes (db) gene result in obesity and diabetes in a syndrome resembling morbid human obesity. Previous data suggest that the db gene encodes the receptor for the obese (ob) gene product, leptin. A leptin receptor was recently cloned from choroid plexus and shown to map to the same 6-cM interval on mouse chromosome 4 as db. This receptor maps to the same 300-kilobase interval as db, and has at least six alternatively spliced forms. One of these splice variants is expressed at a high level in the hypothalamus, and is abnormally spliced in C57BL/Ks db/db mice. The mutant protein is missing the cytoplasmic region, and is likely to be defective in signal transduction. This suggests that the weight-reducing effects of leptin may be mediated by signal transduction through a leptin receptor in the hypothalamus.

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          Journal
          10.1038/379632a0
          8628397

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